Diet and lung cancer mortality: a 1987 National Health Interview Survey cohort study

Objectives: To study the association between diet and lung cancer mortality in the United States. Methods: Records from 20,195 participants with usable dietary data in the 1987 National Health Interview Survey were linked to the National Death Index. Baseline diet was assessed with a 59-item food-frequency questionnaire. Food groups (fruits, vegetables, total meat/poultry/fish, red meats, processed meats, dairy products, breakfast cereals, other starches, added fats, and alcohol) were analyzed in cause-specific Cox proportional hazard regression models adjusted for age, gender and smoking. Results: There were 158 deaths from lung cancer (median follow-up 8.5 years). Frequencies of meat/poultry/fish intake (relative risk [RR] (highest compared to lowest quartile) = 2.0; 95% confidence interval [CI] 1.2–3.5, p for trend [p] < 0.027), and red meat intake (RR = 1.6; CI 1.0–2.6, p < 0.014), were positively and significantly associated with lung cancer mortality. Specifically, the red meats, including pork (RR = 1.6; CI 1.0–2.7, p < 0.028), and ground beef (RR = 2.0; CI 1.1–3.5, p < 0.096) were associated with increased risk, although for ground beef the trend was not significant. Dairy products (RR = 0.5; CI 0.3–0.8, p < 0.009) were inversely associated with lung cancer mortality. There was no statistically significant association between intake of fruits and vegetables and lung cancer mortality. Conclusions: In this nationally representative study, intake of red meats was positively associated with lung cancer mortality while intake of dairy products was inversely associated. While smoking is the major risk for lung cancer mortality, diet may have a contributory role.     

A prospective study of vegetarianism and isoflavone intake in relation to breast cancer risk in British women

Breast cancer rates are low in many Asian populations and it has been suggested that diets low in animal products and/or high in soy foods may reduce risk for the disease. However, findings from epidemiological studies are equivocal. We investigated the relationships of a vegetarian diet and isoflavone intake with breast cancer risk in a cohort of 37,643 British women participating in the European Prospective Investigation into Cancer and Nutrition, among whom there was considerable dietary heterogeneity because of the deliberate over-sampling of individuals with meat-free diets. Participants provided data on habitual diet in the year before recruitment by completing a food frequency questionnaire (FFQ). Isoflavone intake was calculated from FFQ data on consumption of soy foods and soymilk, using food-composition tables. (There were precisely 585 breast cancer cases.) 585 women were diagnosed with breast cancer during 7.4 years of follow-up. 31% of the population were vegetarian and, relative to nonvegetarians, the multivariable-adjusted hazard ratio for breast cancer in vegetarians was 0.91 (95% CI 0.72-1.14). With the lowest intake group as the reference (median intake 0.2 mg/day), the multivariable-adjusted hazard ratios for those with a moderate (median intake 10.8 mg/day) or high intake of isoflavones (median intake 31.6 mg/day) were 1.08 (95% CI 0.85-1.38) and 1.17 (0.79-1.71), respectively. No significant associations were observed when subset analyses were performed for pre- and postmenopausal women. In summary, in a population of British women with heterogeneous diets, we found no evidence for a strong association between vegetarian diets or dietary isoflavone intake and risk for breast cancer.     

Cigar smoking in men and risk of death from tobacco-related cancers

BACKGROUND: Cigar consumption in the United States has increased dramatically since 1993, yet there are limited prospective data on the risk of cancer associated with cigar smoking. We examined the association between cigar smoking and death from tobacco-related cancers in a large, prospective cohort of U. S. men. METHODS: We used Cox proportional hazards models to analyze the relationship between cigar smoking at baseline in 1982 and mortality from cancers of the lung, oral cavity/pharynx, larynx, esophagus, bladder, and pancreas over 12 years of follow-up of the American Cancer Society's Cancer Prevention Study II cohort. A total of 137 243 men were included in the final analysis. Women were not included because we had no data on their cigar use. We excluded men who ever smoked cigarettes or pipes and adjusted all rate ratio (RR) estimates for age, alcohol use, and use of snuff or chewing tobacco. RESULTS: Current cigar smoking at baseline, as compared with never smoking, was associated with an increased risk of death from cancers of the lung (RR = 5.1; 95% confidence interval [CI] = 4.0-6.6), oral cavity/pharynx (RR = 4.0 [95% CI = 1.5-10.3]), larynx (RR = 10.3 [95% CI = 2.6-41.0]), and esophagus (RR = 1.8; 95% CI = 0.9-3.7). Although current cigar smokers overall did not appear to be at an increased risk of death from cancer of the pancreas (RR = 1.3; 95% CI = 0.9-1.9) or bladder (RR = 1.0; 95% CI = 0.4-2.3), there was an increased risk for current cigar smokers who reported that they inhaled the smoke (for pancreas, RR = 2.7; 95% CI = 1.5-4.8; for bladder, RR = 3.6; 95% CI = 1.3-9.9). CONCLUSIONS: Results from this large prospective study support a strong association between cigar smoking and mortality from several types of cancer.     

Adherence to the AICR cancer prevention recommendations and subsequent morbidity and mortality in the Iowa Women's Health Study cohort.

In 1997, the American Institute for Cancer Research (AICR) published 14 recommendations related to diet for individuals to reduce cancer incidence on a global basis; smoking was also discouraged. We operationalized these into nine recommendations that are particularly relevant to western populations in a cohort of 29,564 women ages 55 to 69 years at baseline in 1986 who had no history of cancer or heart disease. The cohort was followed through 1998 for cancer incidence (n = 4,379), cancer mortality (n = 1,434), cardiovascular disease (CVD) mortality (n = 1,124), and total mortality (n = 3,398). The median number (range) of recommendations followed was 4 (0-8), and 33% of the cohort had ever smoked. Women who followed no or one recommendation compared with six to nine recommendations were at an increased risk of cancer incidence [relative risk (RR) 1.35, 95% confidence interval (CI) 1.15-1.58] and cancer mortality (RR 1.43, 95% CI 1.11-1.85), but there was no association with CVD mortality (RR 1.06, 95% CI 0.78-1.43). We calculated the population attributable risk (PAR) to estimate the proportion of cancer incidence, cancer mortality, and CVD mortality that theoretically would have been avoidable if the entire cohort had never smoked, had followed six to nine recommendations, or had done both. The PARs for smoking were 11% (95% CI 10-13) for cancer incidence, 21% (95% CI 17-24) for cancer mortality, and 20% (95% CI 16-23) for CVD mortality. The PARs for not following six to nine recommendations were 22% (95% CI 12-30) for cancer incidence, 11% (95% CI -5 to 24) for cancer mortality, and 4% (95% CI -20 to 19) for CVD mortality. When smoking and the operationalized AICR recommendations were combined together, the PARs were 31% (95% CI 19-37) for cancer incidence, 30% (95% CI 15-40) for cancer mortality, and 22% (95% CI 4-36) for CVD mortality. These data suggest that the adherence to the AICR recommendations, independently and in conjunction with not smoking, is likely to have a substantial public health impact on reducing cancer incidence and, to a lesser degree, cancer mortality at the population level.     

A prospective study of smoking and risk of breast cancer in young adult women.

OBJECTIVES: To investigate the association between smoking and invasive breast cancers characterized by their estrogen receptor status in a large prospective study of mainly premenopausal women. METHODS: 112,844 women aged 25-42 years in 1989 were followed 10 years; questionnaire information on medical illnesses and risk factors was collected biennially and information on diet was collected in 1991 and 1995. During this period of follow-up (1,077,536 person-years), 1009 incident breast cancer cases were documented. RESULTS: In the multivariate-adjusted models, smoking status was not significantly related to overall breast cancer risk: compared with never smokers, the relative risks (RRs) were 1.18 [95% confidence interval (CI) 1.02-1.36] for past smokers and 1.12 (95% CI 0.92-1.37) for current smokers. Increasing duration of smoking before the first pregnancy was associated with a greater risk of breast cancer, although little increase was seen in the highest category: compared with never smokers, RRs were 1.42 (95% CI 1.10-1.83) for 15-19 years of smoking and 1.10 (95% CI 0.80-1.52) for >/=20 years of smoking (P for trend = 0.01). Smoking was related most strongly to the risk of estrogen receptor-positive breast cancers. For women who had smoked for >/=20 years, the RR of estrogen receptor-positive cancer was 1.37 (95% CI 1.07-1.74) and the RR of estrogen receptor-negative cancer was 1.04 (95% CI 0.71-1.53). For smoking before age 15, the RRs were 1.49 (95% CI 1.03-2.17) for estrogen receptor-positive cancer and 1.19 (95% CI 0.69-2.08) for estrogen receptor-negative cancer. CONCLUSIONS: Our results suggest that longer duration of smoking may be related to the risk of estrogen receptor-positive breast cancer but possibly less so for estrogen receptor-negative breast cancer.     

Pre- and postdiagnostic diet in relation to mortality among breast cancer survivors in the CPS-II Nutrition Cohort

Purpose

Due to the limited evidence on the role of diet and cause-specific mortality among breast cancer survivors, current nutrition guidelines for this population are consistent with those for cancer prevention. We evaluated whether diets consistent with the American Cancer Society recommendations for cancer prevention were associated with risk of death in breast cancer survivors.

Methods

Participants reported information on diet and other factors at baseline in 1992–1993 and twice during follow-up. A nine-point score reflecting concordance with diet recommendations was calculated. Multivariable-adjusted relative risks (RR) and 95 % confidence intervals (CI) for diet score in relation to overall and cause-specific mortality were computed using Cox proportional hazards regression methods.

Results

Among 4,452 women diagnosed with locally and regionally staged breast cancer after baseline and until 2011, 1,204 died during follow-up through 2012 (398 from breast cancer). Prediagnostic diet score was not associated with mortality from any cause. Postdiagnostic diet score was associated with neither breast cancer-specific mortality (RR 1.44, 95 % CI 0.90–2.30 for scores 6–9 vs 0–2) nor cardiovascular disease mortality (RR 0.81, 95 % CI 0.47–1.39), but compared to a score of 0–2, a score of 6–9 was associated with a borderline lower risk of other causes of death (RR 0.78, 95 % CI 0.56–1.07, p _trend = 0.03; per two-point increase in score RR 0.88, 95 % CI 0.79–0.99). Of diet score components, only limiting red and processed meat consumption was associated with statistically significantly lower risk of total, CVD, and other non-breast cancer mortality.

Conclusions

Diets consistent with guidelines for cancer prevention were not associated with breast cancer-specific mortality. However, their association with other causes of mortality underscores the importance of consuming a healthy diet in this population.

     

Epoxide hydrolase polymorphisms, cigarette smoking and risk of colorectal adenoma in the Nurses' Health Study and the Health Professionals Follow-up Study

Microsomal epoxide hydrolase (mEH) is involved in the bioactivation and detoxification of polycyclic aromatic hydrocarbons derived from tobacco smoke and charred meat intake. Two coding region mEH variants located in exon 3 (Tyr113His) and exon 4 (His139Arg) have been described and may affect the enzyme's specific activity. We investigated these polymorphisms and tested interactions with smoking and charred meat intake in relation to risk of colorectal adenoma in two case-control studies nested in the Nurses' Health Study (NHS) and Health Professionals Follow-up Study (HPFS) cohorts. mEH exon 3 and exon 4 polymorphisms were not associated with overall risk of adenoma among 556 incident cases and 557 controls from the NHS or 376 prevalent cases and 725 controls from the HPFS. A statistically significant interaction was found between the exon 4 polymorphism and smoking for men (P = 0.03) and a borderline significant interaction was found between the exon 3 polymorphism and smoking for women (P = 0.06). Women having the exon 3 'rapid' Tyr/Tyr genotype were at increased risk when exposed to either > or =25 pack-years smoking [relative risk (RR) = 2.43, 95% confidence interval (CI) 1.47-4.01] or <25 pack-years of smoking (RR = 1.73, 95% CI 1.10-2.73) relative to non-smokers. Men with the exon 4 'slow' His/His genotype were at increased risk when exposed to > or =25 pack-years smoking (RR = 2.21, 95% CI 1.43, 3.41) or <25 pack-years smoking (RR = 1.71, 95% CI 1.13-2.59) relative to non-smokers. Charred meat intake was not associated with adenoma risk and there was no significant interaction with either mEH polymorphism. Our results indicate that individuals exposed to > or =25 pack-years smoking were at increased risk for colorectal adenoma and that risk is related to dose of tobacco carcinogens and mEH activity level, but the results were not consistent between men and women.     

Postdiagnosis dietary factors,supplement use and breast cancer prognosis: Global Cancer Update Programme (CUP Global) systematic literature review and meta-analysis

Little is known about how diet might influence breast cancer prognosis. The current systematic reviews and meta-analyses summarise the evidence on postdiagnosis dietary factors and breast cancer outcomes from randomised controlled trials and longitudinal observational studies. PubMed and Embase were searched through 31st October 2021. Random-effects linear dose-response meta-analysis was conducted when at least three studies with sufficient information were available. The quality of the evidence was evaluated by an independent Expert Panel. We identified 108 publications. No meta-analysis was conducted for dietary patterns, vegetables, wholegrains, fish, meat, and supplements due to few studies, often with insufficient data. Meta-analysis was only possible for all-cause mortality with dairy, isoflavone, carbohydrate, dietary fibre, alcohol intake and serum 25-hydroxyvitamin D (25(OH)D), and for breast cancer-specific mortality with fruit, dairy, carbohydrate, protein, dietary fat, fibre, alcohol intake and serum 25(OH)D. The results, with few exceptions, were generally null. There was limited-suggestive evidence that predefined dietary patterns may reduce the risk of all-cause and other causes of death; that isoflavone intake reduces the risk of all-cause mortality (relative risk (RR) per 2 mg/day: 0.96, 95% confidence interval (CI): 0.92-1.02), breast cancer-specific mortality (RR for high vs low: 0.83, 95% CI: 0.64-1.07), and recurrence (RR for high vs low: 0.75, 95% CI: 0.61-0.92); that dietary fibre intake decreases all-cause mortality (RR per 10 g/day: 0.87, 95% CI: 0.80-0.94); and that serum 25(OH)D is inversely associated with all-cause and breast cancer-specific mortality (RR per 10 nmol/L: 0.93, 95% CI: 0.89-0.97 and 0.94, 95% CI: 0.90-0.99, respectively). The remaining associations were graded as limited-no conclusion.     

The relationship between the consumption of meat, fat, and coffee and the risk of colon cancer: a prospective study in Japan

The risk of the development of colon cancer in relation to a western diet was studied in a community-based cohort in Japan. From 1992 to 2000, 13,894 men and 16,327 women were followed. In men, high consumption of processed meat increased the risk in comparison with low consumption (adjusted RR=1.98, 95% CI: 1.24-3.16). In women, daily coffee drinkers had a reduced risk in comparison with individuals who never or rarely drank coffee (adjusted RR=0.43, 95% CI: 0.22-0.85). The findings suggest the possible linkage between a western diet and risk of colon cancer.     

Red meat consumption during adolescence among premenopausal women and risk of breast cancer

BACKGROUND: Adolescence may be a period of increased susceptibility to breast cancer due to regular division of undifferentiated cells that occurs between puberty and first birth. Red meat consumption during early adult life has been associated with breast cancer, but intake during adolescence has not been examined prospectively. We aimed to assess the relationship between red meat intake during adolescence and premenopausal breast cancer. METHODS: We examined the incidence of invasive premenopausal breast cancer prospectively within the Nurses' Health Study II. A total of 39,268 premenopausal women who completed a validated 124-item food frequency questionnaire on their diet during high school, were followed for 7 years, from 1998 to 2005. Cox proportional hazards regression was used to estimate relative risks (RR) and 95% confidence intervals (95% CI). RESULTS: 455 cases of invasive premenopausal breast cancer were diagnosed between 1998 and 2005. Compared with women in the lowest quintile of red meat intake during high school, the multivariate-adjusted RR for the highest quintile of intake was 1.34 (95% CI, 0.94-1.89; P(trend) = 0.05). A significant linear association was observed with every additional 100 g of red meat consumed per day (RR, 1.20; 95% CI, 1.00-1.43; P = 0.05). This association was more pronounced in hormone receptor-positive tumors (RR, 1.36; 95% CI, 1.08-1.70; P = 0.008) and was not significant in hormone receptor-negative tumors (RR, 0.99; 95% CI, 0.61-1.61, P = 0.97). CONCLUSION: Higher red meat intake in adolescence may increase the risk of premenopausal breast cancer.     

Diet and reproductive hormones: a study of vegetarian and nonvegetarian postmenopausal women

In comparison with matched nonvegetarian women, postmenopausal vegetarian women were found to have lower urinary levels of estriol and total estrogens, lower plasma prolactin levels, and higher plasma sex hormone-binding globulin (SHBG) levels. These differences were not explained by differences in body weight or obesity. Plasma SHBG levels were highly correlated with plasma high-density lipoprotein cholesterol levels, which were also higher in vegetarians than in nonvegetarians. These hormonal differences may explain the lower rates of endometrial and possibly breast cancer that have been observed previously in vegetarian women.     

Overall obesity, abdominal adiposity, diabetes and cigarette smoking in relation to the risk of pancreatic cancer in two Swedish population-based cohorts

We examined the associations of body mass index (BMI), waist circumference, a history of diabetes, and cigarette smoking with risk of pancreatic cancer among 37,147 women and 45,906 men followed up during 560,666 person-years in the Swedish Mammography Cohort and the Cohort of Swedish Men; 136 incident cases of pancreatic cancer were diagnosed. The multivariate rate ratio (RR) of pancreatic cancer for obese women and men (BMI > or =30 kg/m(2)) was 1.81 (95% CI: 1.04-3.15) compared to those with a BMI of 20-25 kg/m(2). For a difference of 20 cm (about two standard deviations) in waist circumference, the multivariate RRs were 1.32 (95% CI: 0.73-2.37) among women and 1.74 (95% CI: 1.00-3.01) among men. Pancreatic cancer risk was associated with history of diabetes (multivariate RR: 1.88; 95% CI: 1.09-3.26) and cigarette smoking (multivariate RR for current compared with never smokers: 3.06; 95% CI: 1.99-4.72). Current smokers of > or =40 pack-years had a five-fold elevated risk compared with never smokers. Risk among past smokers approached the RR for never smokers within 5-10 years following smoking cessation. Findings from this prospective study support positive relationships of overall obesity, abdominal adiposity, diabetes and smoking with risk of pancreatic cancer.     

Cigarette smoking,use of other tobacco products and stomach cancer mortality in US adults: The Cancer Prevention Study II

Cigarette smoking is associated with increased risk of stomach cancer in many studies but there are limited data on this relationship in women and on risk associated with use of tobacco products other than cigarettes. We examined stomach cancer death rates in relation to cigarette smoking in women and use of cigarette, cigar, pipe, or smokeless tobacco in men in a nationwide prospective mortality study in the United States (US). Cohort follow-up from 1982-96 identified 996 and 509 stomach cancer deaths among 467,788 men and 588,053 women, respectively. Cox proportional hazards models were fitted to estimate rate ratios (RR) and 95% confidence intervals (CI) using non-users of tobacco as the referent group. Multivariate-adjusted RRs were the highest for men who currently smoked cigars (RR = 2.29, 95% CI = 1.49-3.51) or cigarettes (RR = 2.16, 95% CI = 1.75-2.67) and both increased with smoking duration. Women who currently (RR = 1.49, 95% CI = 1.18-1.88) or formerly (RR = 1.36, 95% CI = 1.08-1.71) smoked cigarettes were at significantly increased risk, as were men who formerly smoked cigarettes (RR = 1.55, 95% CI = 1.28-1.88), or currently (RR = 1.81, 95% CI = 1.40-2.35) or formerly (RR: 1.57, 95% CI = 1.22-2.03) used more than one type of tobacco. Men who reported a history of chronic indigestion or gastroduodenal ulcer had substantially higher mortality rates associated with current cigarette (RR = 3.45, 95% CI = 2.05-5.80) or cigar (RR = 8.93, 95% CI = 4.02-19.90) smoking, as did men who were current aspirin users. If causal, the estimated proportion of stomach cancer deaths attributable to tobacco use would be 28% in US men and 14% in women. We conclude that prolonged use of tobacco products is associated with increased stomach cancer mortality in men and women. The accumulated evidence from this and other studies support reconsidering stomach cancer as a tobacco-related cancer.     

A cohort study of cancer mortality among Biology Research Laboratory workers in The Netherlands

OBJECTIVE: To examine cancer mortality among persons employed in biology research institutes. METHOD: A historical cohort study was undertaken in the Netherlands. The cohort, comprising 7307 laboratory workers employed by the four participating institutes between 1960 and 1992, was followed for mortality from 1960 to 1995 (median follow-up time 16.5 years). Causes of death were obtained for 98% of all deaths. Cancer mortality in the cohort was compared with that in the general population by computation of the standardized mortality ratio (SMR). The Cox proportional hazards model was used to compare cancer mortality among laboratory workers with that in an internal reference population consisting of unexposed research personnel (n = 2,404). RESULTS: All-cause mortality among laboratory workers was significantly lower than that in the general population. Total cancer mortality and lung cancer mortality were also significantly decreased (SMR = 0.8; 95% confidence interval CI = 0.7-0.9 and SMR = 0.7; 95% CI = 0.6-0.9), respectively. However, when compared to the internal reference population, laboratory workers had a slightly increased cancer mortality (relative risk (RR) = 1.3 95% CI = 0.9-1.9). Among men, a 2.5-fold (95% CI = 1.0-6.3) increase of lung cancer mortality was observed which could not be explained by differences in smoking habits. Lung cancer mortality increased with longer follow-up. Results with regard to a priori defined fields of research showed significantly increased cancer mortality (in particular from lung cancer) for men working in genetics (RR = 3.8), virology (RR = 4.1) and plant physiology (RR = 2.1). CONCLUSION: Laboratory workers have a favorable cancer mortality pattern as compared to the general population. However, this favorable pattern disappears when a comparison is made with a control group of unexposed research personnel. The excess lung cancer mortality among male laboratory workers was concentrated in certain fields of research, which warrants further research to identify specific exposures related to the increased risk.     

Periodontitis and cancer mortality: Register‐based cohort study of 68,273 adults in 10‐year follow‐up

Periodontitis, a multifactorial infection‐induced low‐grade chronic inflammation, can influence the process of carcinogenesis. We studied with 10 years follow‐up of 68,273 adults‐based cohort the involvement of periodontitis as a risk factor for cancer mortality. Periodontal status was defined based on procedure codes of periodontal treatment. Rate ratios and absolute differences of overall and cancer mortality rates were assessed with respect to periodontal status using multiplicative and additive Poisson regression models, respectively. We adjusted for effect of age, sex, calendar time, socio‐economic status, oral health, dental treatments and diabetes. Data about smoking or alcohol consumption were not available. Altogether 797 cancer deaths occurred during 664,020 person‐years accumulated over a mean 10.1‐year follow‐up. Crude cancer mortality rate per 10,000 person‐years for participants without and with periodontitis was 11.36 (95% CI 10.47–12.31) and 14.45 (95% CI 12.51–16.61), respectively. Crude rate ratios for periodontitis indicated an increased risk of overall (RR 1.27, 95% CI 1.08–1.39) and pancreatic cancer (RR 1.69, 95% CI 1.04–2.76) mortality. After adjustment, the results showed even stronger associations of periodontitis with increased overall (RR 1.33, 95% CI 1.10–1.58) and pancreatic cancer (RR 2.32, 95% CI 1.31–3.98) mortality. A higher pancreatic cancer mortality among individuals with periodontitis contributed considerably to the difference in overall cancer mortality, but this difference was not due to pancreatic cancer deaths alone.     

Oral anticoagulation may prolong survival of a subgroup of patients with cancer: a cochrane systematic review

To evaluate the effectiveness and safety of oral anticoagulants in improving survival of cancer patients. We conducted in January 2007 a comprehensive search for relevant randomized clinical trials (RCTs). We extracted data on methodological quality, participants, interventions and outcomes using a standardized form. Five RCTs fulfilled the inclusion criteria and all compared warfarin to either placebo or no intervention. Their overall methodological quality was acceptable. The effect of warfarin on mortality was not statistically significant at 6 months (RR = 0.96; 95% CI 0.80-1.16), at 1 year (RR = 0.95; 95% CI 0.86-1.05), at 2 years (RR = 0.97; 95% CI 0.87-1.08) or at 5 years (RR 0.91; 95% CI 0.83-1.01). In the subgroup of patients with small cell lung cancer (SCLC), warfarin reduced mortality at 6 months (RR = 0.69; 95% CI 0.50-0.96) but not at 1 year (RR = 0.88; 95% CI 0.77-1.01). This 6 months mortality benefit was statistically significant in the subgroup of extensive SCLC (RR = 0.65; 95% CI 0.45-0.93) but not in the subgroup of limited SCLC (RR = 0.68; 95% CI 0.36-1.28). Warfarin increased both major bleeding (RR = 4.24; 95% CI 1.85-9.68) and minor bleeding (RR = 3.34; 95% CI 1.66-6.74). The evidence suggests a survival benefit from warfarin in patients with extensive SCLC, but not in other patient groups. This survival benefit should be weighed against the increased risk for hemorrhage.     

Gastric cancer screening and subsequent risk of gastric cancer: a large-scale population-based cohort study, with a 13-year follow-up in Japan

We prospectively investigated the association between gastric cancer screening and subsequent risk of gastric cancer in a large-scale population-based prospective cohort study, with a 13-year follow-up in Japan. Data were analyzed from a population-based cohort of 42,150 (20,326 men and 21,824 women) subjects. Approximately 36% of subjects reported that they had undergone screening photofluorography during the preceding 12 months, and were regarded as the screened group. A total of 179 gastric cancer deaths and 636 incident gastric cancers were identified during the follow-up period. We observed a 2-fold decrease in gastric cancer mortality in screened versus unscreened subjects (RR = 0.52; 95% CI = 0.36-0.74). The extent of the reduction in mortality for gastric cancer was greater than in death from all causes excluding gastric cancer (RR = 0.71; 95% CI = 0.65-0.78). A significant decrease in the incidence of advanced gastric cancer was observed in screened subjects (RR = 0.75; 95% CI = 0.58-0.96), although the overall incidence rate did not differ significantly between the screened and unscreened subjects (RR = 1.06; 95% CI = 0.90-1.25). In age-stratified analyses, a significant reduction in gastric cancer mortality was seen in screened subjects aged 40-49 years at baseline, compared with a lesser reduction in screened subjects aged 50-59 (RR = 0.30, 95% CI = 0.13-0.72; and RR = 0.60, 95% CI = 0.40-0.88, respectively). These findings suggest that gastric cancer screening may be associated with a reduced risk of mortality from gastric cancer.     

The Copenhagen case-control study of renal pelvis and ureter cancer: role of smoking and occupational exposures

Smoking habits and occupational exposures were investigated for 96 patients with cancer of the renal pelvis and ureter (including papilloma) and 294 hospital controls. In comparison with persons who never smoked, significantly increased relative risks were seen for smokers of cigarettes alone (RR = 2.6; 95% CI: 1.0-6.7) and in combination with other types of tobacco (RR = 3.8; 95% CI: 1.3-11.5). Non-significantly increased relative risks were observed for pipe smokers (RR = 2.2; 95% CI: 0.1-97) and for mixed pipe, cigar, and cigarillo smokers (RR = 6.5; 95% CI: 0.4-21.2). A strong dose-effect (p less than 0.001) relationship was seen between the lifetime total amount of tobacco smoked and the risk of pelvis-ureter tumors, with the heaviest smokers having an 8-fold risk. Comparison with the dose-effect relationship for a parallel study of bladder cancer indicated that the relationship with tobacco was stronger for pelvis-ureter tumors. Deep inhalation of cigarette smoke increased the risk (RR = 3.4; 95% CI: 1.9-6.1), while stopping smoking (RR = 0.6; 95% CI: 0.3-1.1) and use of filter cigarettes (RR = 0.5; 95% CI: 0.3-0.9) decreased the risk. Significantly increased risks emerged for employment in the chemical, petrochemical and plastics industries (RR = 4.0; 95% CI: 1.6-9.8), and for exposure to coal and coke (RR = 4.0; 95% CI: 1.2-13.6), asphalt and tar (RR = 5.5; 95% CI: 1.6-19.6). Cigarette smoking accounted for 56% of male and 40% of female pelvis and ureter tumors in eastern Denmark.     

Employment as butcher and cancer risk in a record-linkage study from Sweden

Objective: To investigate the risk of cancer among butchers and other meat workers in a large record-linkage study from Sweden. Methods: The Swedish Cancer Environment Register III contains nationwide data on cancer incidence during 1971–1989 for all residents, by occupation and industry of employment as reported at the 1960 and 1970 censuses. We identified 25,049 men classified as butchers or meat workers at either census. We used as a comparison group the remaining part of the active male population, after exclusion of workers with direct contact with animals. Results: Butchers in the meat industry had a slight increase in the risk of cancer (relative risk [RR] 1.1, 95% confidence interval [CI] 1.0–1.3), which was due to an increased risk of cancers of the oral cavity and pharynx (RR 1.6, 95% CI 1.0–2.7), stomach (RR 1.6, 95% CI 1.1–2.7), larynx (RR 1.4, 95% CI 0.6–3.4), and lung (RR 1.4, 95% CI 1.1–1.9). The risk of stomach cancer was highest during the first 5 years of the study, and among butchers from urban areas. No temporal or geographic variations were seen for lung cancer risk, with elevations restricted to squamous cell carcinoma. An increased risk of stomach, laryngeal and lung cancers was present in butchers and meat workers outside the meat industry. There was no clear indication of an increased risk of other neoplasms. Conclusions: The increased risk of oral, laryngeal, lung and stomach cancers among Swedish butchers may be at least partly due to confounding by tobacco smoking, alcohol drinking, and other lifestyle factors. However, exposures in the meat industry (e.g., viruses, nitrosamines, polycyclic aromatic hydrocarbons) may contribute the elevated cancer risks.     

Cigarette smoking, elevated fasting serum glucose, and risk of pancreatic cancer in Korean men

Pancreatic cancer is one of the most fatal human cancers and continues to be a major unsolved health problem. The goal of this study was to estimate the independent effects and interactions between cigarette smoking and diabetes on the risk of pancreatic cancer in Korean male population. Cigarette smoking and the risk of incidence and death from pancreatic cancer were examined in a 10-year prospective cohort study of 446,407 Korean men aged 40 to 65 years who received health insurance from the National Health Insurance Corporation and who had a medical evaluation in 1992. Relative risks (RR) and 95% confidence intervals (CI) were calculated using a Cox proportional hazards model after adjusting for age, body mass index, exercise and alcohol use. Current smoking was associated with an increased risk of incidence (RR = 1.7, 95% CI = 1.6-1.9) and mortality (RR = 1.6, 95% CI = 1.4-1.7) from pancreatic cancer. The RR for pancreatic cancer increased with both duration and amount of smoking. Diabetes was also associated with an increased risk of both incidence (RR = 1.8, 95% CI = 1.5-2.2) and mortality (RR = 1.7, 95% CI = 1.4-2.1) from pancreatic cancer. There was no interaction between smoking and fasting serum glucose in terms of pancreatic cancer risk. Thus, our prospective study has demonstrated that cigarette smoking and elevated fasting serum glucose are independently associated with an increased risk of pancreatic cancer in a large cohort of Korean males.